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rhTNFR:Fc increases Nrf2 expression via miR-27a mediation to protect myocardium against sepsis injury
Wei-Liang Xue1, Xiaoyan Bai2, Ling Zhang1
1Department of Emergency, The People's Hospital of the Ningxia Hui Autonomous Region, Yinchuan 750000, China.
Objective:
Sepsis is a whole-body inflammation disease and can result in septic shock and multiple organ failure. The previous study demonstrated that miR-27a plays a critical role in inflammation regulation. Here, we investigated that effect and its possible mechanism of rhTNFR:Fc on sepsis treatment.
Methods:
LPS induced sepsis mice model was established. 10 mg/kg rhTNFR:Fc was used to treat sepsis mice by intravenous injection.
Results:
RhTNFR:Fc improved cardiac function of sepsis mice, and markedly decreased miR-27a but increased Nrf2 expression level of myocardium in LPS treated mice. In H9C2 cells, rhTNFR:Fc also increased Nrf2 expression, elevated cell viability and decreased cell apoptosis. However, the effects were reversed by miR-27a mimic. In addition, miR-27a mimic reduced the activity of Nrf2 3'UTR while miR-27a inhibitor elevated enhanced its level.
Conclusion:
rhTNFR:Fc activated Nrf2 pathway to protect myocardium against LPS-induced sepsis injury via miR-27a regulation.
